Objective As estrogen increases visceral hypersensitivity induced by water avoidance stress in female rats,further experiment was designed to determine whether the influence of estrogen involves NR2B.Methods Healthy adult female Wistar rats were bilaterally ovariectomized,and then housed individually.Implantation of cannula into lateral cerebroventricle and electrodes into the abdominal muscle had been done.After 5 days recovery,rats with abnormal behavior and ehctromyography were excluded,finally a total of 48 rats were eligible,and were equipped for abdominal muscle electromyography and submitted to water avoidance stress(WAS).Visceromotor response(VMR)to 20,40,60 and 80 mmHg colorectal distension(CRD)was recorded in rats intracerebroventricular-infused with either 17β-estradiol,normal saline,AP5(NMDA receptor-antagonist)or Ro25-6981(NR2B antagonist).NR2B mRNA in anterior cingulate cortex or dorsal root ganglia were compared by real-time PCR between the rats treated with 17β-estradioI and that with normal saline.Results Bilaterally ovarieetomized rats treated with 17β-estradiol,exhibited more visceral hypersensitivity after WAS than that with normal saline on 40,60 and 80 mmHg CRD(P=0.039,P=0.033,P=O.001).The VMR on 40 and 60 mmHg CRD in 17β-estradiol treated group was not significantly different from that in 17β-estradiol plus Ro25-6981 treated group.Whilst,significant differences of VMR were noted between 17β-estradiol treated group and 17β-estradiol plus Ro25-6981 treated group on 80 mmHg CRD,17β-estradiol treated group and 17β-estradiol plus AP5 treated group on 60,80 nmmHg CRD,respectively.17β-estradiol increased NR2BmRNA in anterior cingulate cortex(0.57±0.41 vs 0.21±0.13,P=0.048),but not in dorsal root ganglia(0.35±0.45 vs 0.38±0.31,P=0.465). Stress-induced visceral hypersensitivity in the hormonally-restored visceral hyper-responsiveness of bilaterally ovariectomized rats was antagonized by AP5 or Ro25-6981.Conclusions Estrogen may be mediated through NR2B activation to enhance visceral sensitivity in female stressed rats,that probably related with the increased expression of NR2B mRNA in anterior cingulate cortex.

Objective: The main ingredients and the inhibitory effects of essential oil of a compound Chinese herbal medicine Weiqi Decoction (WQD) on AGS cell proliferation were to be investigated. Methods: Chemical compounds of WQD essential oil were detected by gas chromatography and mass spectrometry analysis. Cell viability was measured by methyl thiazolyl tetrazolium method. Cell cycle distribution was detected by flow cytometry. Apoptosis and necrosis of AGS cells were determined by Hoechst 33342/propidium iodine staining. Results: Chemical analysis showed that the main ingredients of WQD essential oil were bornylene and 3-n-butylphthalide. Ligustilide, which is the effective compound of Danggui (Radix Angelicae Sinensis), was not detected in WQD essential oil. The essential oil inhibited cell proliferation in a dose- and time-dependent manner, and blocked cell cycle progression at G(2)/M stage. At the concentrations that resulted in significant inhibition of cell proliferation and cell cycle arrest, essential oil induced both apoptosis and necrosis. Conclusion: The results suggest that WQD essential oil contains some effective ingredients for treating chronic atrophic gastritis and functional dyspepsia, and also has an antiproliferative effect on AGS cells through cell cycle arrest and apoptosis promotion in vitro. Therefore, essential oil should be retained as much as possible during stewing this decoction.

Objective To study the therapeutic effects of Bioenterics Intragastric Balloon (BIB) on obesity under gastroscopy.Methods Data of 47 patients treated with Bioenterics Intragastric Balloon under gastrscopy were reviewed from July,2010 to May,2011.Results Weight loss ( mean 15.4 kg ) was successfully achieved in all the patients during 6 months.BMI decreased by 3.2-6.4 kg/m2 ( mean 4.7 kg/m2 ).There was no serious side effect with a better result for obesity according to the follow-up.Conclusion BIB is effective for obesity for noninvasiveness,stable speed of weight loss and less pain.

OBJECTIVETo study the effects and mechanisms of sinensetin on proliferation and apoptosis of human AGS gastric cancer cells.

METHODMTT assay was used to detect the growth inhibition rates of human AGS gastric cancer cells treated with sinsesectin in different concentrations and times. The cell cycle distribution was measured by flow cytometry. The apoptosis was examined by Annexin-FITC/PI staining and DNA fragment analysis. The apoptosis morphology was observed by inverted fluorescence microscope after Hoechst 33342 staining. The protein expressions of p21 and p53 were detected by western blot.

RESULTMTT assay showed that sinensetin inhibited the growth of AGS gastric cancer cells in a dose- and time-dependent manner. Sinensetin blocked AGS cells in G2/ M and increased the apoptosis rates of AGS cells in a dose-dependent manner. DNA ladder was observed in cells treated with 60 micromol x L(-1) sinensetin for 48 h. The typical apoptotic morphological changes including cell nucleus shrinkage, chromatin condensation and apoptotic bodies were observed when treated with different dose of sinensetin. Western blot showed that sinensetin increased expressions of p53 and p21 in a dose-dependent manner.

CONCLUSIONSinensetin could inhibit human AGS gastric cancer cells proliferation and induce cell cycle block in G2/M phase and apoptosis. The up regulation of p53 and p21 protein might be one of the mechanisms.

Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cyclin-Dependent Kinase Inhibitor p21 ; analysis ; Dose-Response Relationship, Drug ; Flavonoids ; pharmacology ; Humans ; Stomach Neoplasms ; drug therapy ; pathology ; Tumor Suppressor Protein p53 ; analysis